Implantable permanent and temporary medical electrical stimulation and/or sensing leads are well known in the fields of cardiac stimulation and monitoring, including cardiac pacing and cardioversion/defibrillation, and in other fields of electrical stimulation or monitoring of electrical signals or other physiologic parameters. In the field of cardiac stimulation and monitoring, the electrodes of epicardial or endocardial cardiac leads are affixed against the epicardium or endocardium, respectively, or inserted therethrough into the underlying myocardium of the heart wall.
It has become possible to reduce endocardial lead body diameters from 10 to 12 French (3.3 to 4.0 mm) down to 2 French (0.66 mm) presently through a variety of improvements in conductor and insulator materials and manufacturing techniques. The lead bodies of such small diameter, 2 French, endocardial leads are formed without a lumen that accommodates use of a stiffening stylet to assist in implantation.
These small diameter endocardial pacing and cardioversion/defibrillation leads are advantageously sized to be advanced into the coronary sinus to locate the distal electrode(s) adjacent to the left atrium or into coronary veins branching from the coronary sinus to locate the distal electrode(s) adjacent to the left ventricle. The distal end of such a coronary sinus lead is advanced through the superior vena cava, the right atrium, the valve of the coronary sinus, the coronary sinus, and, if employed to pace or sense the left ventricle, into a cardiac vein branching from the coronary sinus.
Typically, such small diameter endocardial leads are formed with an active fixation helix that extends distally and axially in alignment with the lead body to a sharpened distal tip and that has a helix diameter substantially equal to the lead body diameter. The fixation helix does not necessarily increase the overall diameter of the endocardial lead and is relatively robust, once the helix is screwed into the myocardium. Typically, but not necessarily, the fixation helix is electrically connected to a lead conductor and functions as a pace/sense electrode. In some cases, the lead body encloses one or more helical coiled or stranded wire conductor and lacks a lumen.
The lead bodies of such small diameter endocardial screw-in leads are so supple and flexible that it is difficult to rotate the lead distal end by application of rotary torque to the lead proximal end unless the lead body remains relatively straight and not confined by contact with vessel walls. This diminished “torqueability” prevents the rotation of the fixation helix at the lead distal end or renders the rotation unreliable once the lead body is advanced through a tortuous pathway and confined by contact against the vessel walls. To the degree that rotation torque can be transmitted from the lead proximal end to the lead distal end, the active fixation helix at the lead distal end can be over-rotated and screwed through the myocardium or under-rotated and not screwed into the myocardium sufficiently. In addition, such lead bodies also possess little if any column strength and lack “pushability”, that is the ability to advance the lead distal end axially when the lead proximal end is pushed axially, particularly when the lead body extends through the tortuous transvenous pathway. Thus, it has been found necessary to use implantation instruments or tools that compensate for the lack of pushability and torqueability of the lead body.
Once the implantation site is reached in coronary vasculature, it is difficult to aim the distal fixation mechanism toward myocardial tissue, and the fixation mechanism may inadvertently be aimed at and deployed outside the myocardium. The pace/sense electrodes may not be in intimate contact with excitable cardiac tissue, resulting in unduly high stimulation thresholds and diminished sensing. Fixation may be achieved temporarily, but fixation may be lost over time resulting in dislodgement of the pace/sense electrode(s). The fixation mechanism may perforate through a coronary vessel wall into the pericardial space resulting in perforation of the vessel.